How can this be? We actually think we’ve got a fair handle on the sorts of evolutionary landscape that can select for negligible senescence. In a nutshell (clamshell?), the idea is that when organisms must compete for real estate against older adults of the same species, they’re under pressure to delay aging as much as possible. In extreme cases, this can result in an evolutionary “arms race” in which aging is entirely eliminated. This has happened mostly in sessile organisms such as trees and clams, but there’s some reason to believe that privileged breeders in eusocial/hive species such as ants and mole rats are under similar evolutionary pressures.

We’re less certain about the molecular specifics of negligible senescence: Granted that situations arise in which natural selection might act to eliminate aging — how would this then be accomplished? In other words, how does evolution drive delays in the aging process?

The ocean quahog Arctica islandica is the longest-lived of all bivalve and molluscan species on earth. Animals close to 400 years are common and reported maximum live span around Iceland is close to 400 years. High and stable antioxidant capacities are a possible strategy to slow senescence and extend lifespan and this study has investigated several antioxidant parameters and a mitochondrial marker enzyme in a lifetime range spanning from 4-200 years in the Iceland quahog. In gill and mantle tissues of 4-192 year old A. islandica, catalase, citrate synthase activity and glutathione concentration declined rapidly within the first 25 years, covering the transitional phase of rapid somatic growth and sexual maturation to the outgrown mature stages (∼32 years). Thereafter all three parameters kept rather stable levels for 150 years. In contrast, superoxide dismutase activities maintained high levels throughout life time. These findings support the ‘Free Radical-Rate of Living theory’, antioxidant capacities of A.islandica are extraordinarily high and thus may explain the species long life span.

So: long-lived molluscs have much higher antioxidant capacities than short-lived molluscs, suggesting a mechanism by which their much slower (possibly “negligible” senescence) might have evolved.

Because correlation ≠ causation, however, this does not constitute proof — for that, we’d need to beef up the superoxide dismutase levels of one of the shorter-lived clams to A. islandica levels, and observe the effect on lifespan. (Anyone for a 500-year doctoral thesis? You’d better get started today.)

Another point: No defense based on prevention of damage (in this case, oxidation of protein and DNA) is 100% efficient. Assuming that protein and DNA oxidation contributes to the aging process in bivalves, even a very efficient SOD system will eventually allow oxidative adducts to accumulate to dangerous (i.e., gerontogenic) levels. If A. islandica is truly biologically ageless, then it must also have efficient repair systems in order to reverse, as opposed to merely prevent, oxidative damage. Then again, if this clam is simply aging very, very slowly, then maybe high levels of SOD are enough. Which is it? Only time will tell. (In the meantime, I think I have a side project for the very patient thesis student we met in the previous paragraph.)